Based on preliminary results showing that both blood pressure and plasma glucose can be elevated concurrently during electrical stimulation of the ventromedial hypothalamus, studies are proposed to test the hypothesis that sympathetic hyperactivity resulting from hypothalamic dysfunction is a common denominator in the etiology of experimental diabetes and hypertension. Initial experiments will establish the time-course of pressor and hyperglycemic effects produced by treatment with alloxan or streptozotocin in awake normotensive rats; similar experiments would later be done in other rats with spontaneous, neurogenic, renal, or Doca-salt hypertension. Pressor responsiveness to injected drugs like norepinephrine, angiotensin, serotonin, or vasopressin, and to electrical stimulation of various hypothalamic centers, will be recorded following induction of experimental diabetes. The extent of sympathetic involvement under these conditions will be estimated by recording sympathetic nerve activity as well as responses to different autonomic blocking drugs. As a means for inducing sustained sympathetic hyperactivity in awake rats, chronic hypothalamic stimulation (14 hours daily for several weeks) will be done, and periodic measurement of blood pressure and plasma glucose would then indicate whether resulting elevations can be maintained. In other experiments, chronic hypothalamic stimulation of rats pretreated with alloxan would be done to determine if the cardiovascular sequelae of diabetes would be aggravated.